Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01034 (cystatin C)
 3,397 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estimation of the glomerular filtration rate (GFR) is essential for the evaluation of patients with chronic kidney disease (CKD). The Cockcroft-Gault (CG) and modification of diet in renal disease (MDRD) formulas are serum creatinine-based equations, and the most widely used tests for renal function. Recently, serum cystatin C-based equations were proposed as markers for estimation of GFR. The present study compares our serum cystatin C-based equation (cystatin C formula) and serum creatinine-based equations for a large group of patients with CKD. In this study, 592 adult patients with CKD were enrolled. In each patient, serum creatinine was determined and creatinine clearance was calculated using the CG and MDRD formulas. The serum cystatin C was determined by an immunonephelometric method and our own cystatin C formula (GFR = 90.63 x cystatin C-1.192) for estimation of GFR was developed. GFR was measured using 51CrEDTA clearance, and the correlation, accuracy, bias and precision were determined. Ability to correctly estimate the patient's GFR with different equations compared to gold standard below and above 60 ml/min/1.73 m2; was analyzed. The mean 51CrEDTA clearance was 47 ml/min/1.73 m2, the mean serum creatinine was 269 micromol/l and the mean serum cystatin C was 2.68 mg/l. Statistically significant correlation between 51CrEDTA clearance with the CG (r = 0.861) and MDRD (r = 0.909) formulas and the cystatin C formula (r = 0.899) was found. The receiver operating characteristic (ROC) curve analysis (cut-off for GFR 60 ml/min/1.73 m2) showed that the cystatin C formula had a significantly higher diagnostic accuracy than the CG formula (p < 0.003). All equations underestimated the measured GFR and lacked precision. Analysis of ability to correctly predict the patient's GFR below or above 60/ml/min/1.73 m2 showed a higher prediction for the cystatin C formula than the MDRD formula (91.6 versus 84.1%, p < 0.0005) and a higher prediction trend than the CG formula (91.6 versus 88.3%, p = 0.078). Our results indicate that serum cystatin C-based equation is a reliable marker of GFR with a very high diagnostic accuracy and ability to predict patients with CKD and GFR under 60/ml/min/1.73 m2.
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PMID:Serum cystatin C-based equation compared to serum creatinine-based equations for estimation of glomerular filtration rate in patients with chronic kidney disease. 1879 43

The onset of diabetic nephropathy is characterised by a rise in albumin excretion rate (AER) and/or a transient rise in glomerular filtration rate (GFR) (hyperfiltration). Without intervention AER increases exponentially and there is a linear decrease in GFR after onset of overt nephropathy. In overt nephropathy, AER is a predictor of decline in GFR and the early AER response to antihypertensive therapy correlates with long-term decline in GFR. AER can be measured by immunoassay or by other techniques including HPLC. However, HPLC assays result in higher levels of AER in normal subjects compared with immunoassayable AER. Recent data suggest that there are distinct albuminuric and non-albuminuric pathways to renal impairment in type 1 and type 2 diabetes. In type 2 diabetes, the non-albuminuric pathway may explain a decline in GFR to <60 ml/min/1.73 m(2) in approximately one in four subjects after accounting for the use of renin angiotensin system inhibitors. In established nephropathy (chronic kidney disease (CKD) stages 3 and 4), plasma cystatin C based estimates of GFR are marginally superior to creatinine based estimates. However, cystatin C clearly outperforms creatinine based estimates of GFR decline at GFR levels >60 ml/min/1.73 m(2) (CKD stages 1 and 2). Other potential markers of progression of diabetic nephropathy include transforming growth factor beta (TGFbeta) and connective tissue growth factor (CTGF). However, long-term studies are needed to define their roles as markers of progression. Diabetic nephropathy is likely to be more susceptible to intervention at an early stage and accurate estimation of GFR is already possible with cystatin C. However, improved formulas for estimating GFR based on using creatinine or other markers are still required, because this may still provide the most cost effective approach applicable to existing clinical practice.
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PMID:New and old markers of progression of diabetic nephropathy. 1893 92

The estimation of the glomerular filtration rate (GFR) is essential for the evaluation of patients with kidney disease and for the treatment of patients with medications that are eliminated by the kidneys. Plasma cystatin C has been shown in several studies to be superior to plasma creatinine for the estimation of GFR. However, there is limited information on the circadian variation of cystatin C and estimated GFR using cystatin C (eGFR(CystC)) or "The Modification of Diet in Renal Disease Study" (MDRD) (eGFR(MDRD)) equations. We studied the circadian variation of cystatin C and creatinine during night- and day-sleep conditions in seven healthy volunteers. Serum samples were collected every hour (48 samples per individual) to evaluate the effect of different sampling times on the test results. The median intra-individual coefficients of variations for the studied markers were 4.2% for creatinine, 4.7% for eGFR(MDRD), 5.5% for cystatin C, and 7.7% for eGFR(CystC). Neither cystatin C nor creatinine differed significantly between the night- and day-sleep conditions. Cystatin C differed significantly with time of day (p=.0003), but this was not the case for creatinine (p=.11). The circadian variation of cystatin C was minor. Small but significant increases in creatinine values and a decrease of eGFR(MDRD) were observed after food intake. Thus, cystatin C and creatinine sampling does not have to be restricted to specific times of the day.
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PMID:Circadian variability of cystatin C, creatinine, and glomerular filtration rate (GFR) in healthy men during normal sleep and after an acute shift of sleep. 1900 4

We examined usefulness of serum cystatin C to detect chronic kidney disease (CKD) stage >or=3, which was defined by Modification of Diet in Renal Disease formula. Serum cystatin C could detect CKD stage >or=3 with high efficacy in 289 Japanese patients with type 2 diabetes and nephropathy.
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PMID:Usefulness of serum cystatin C in Japanese patients with type 2 diabetes mellitus and nephropathy. 1911 14

Paraoxonase 1 (PON1) has been reported to be associated with proteinuria in subjects with type 2 diabetes mellitus (T2DM). Plasma cystatin C is more accurate than creatinine for identifying stage 3 kidney disease in T2DM. We tested the hypothesis that PON1 and cystatin C would be associated in T2DM subjects from an Aboriginal Canadian community, who are at high risk for the development of nephropathy. PON1 A(-162)G and PON2 Ala148Gly genotypes, cystatin C, HbA1c, high density lipoprotein cholesterol (HDLC), waist circumference (waist), and duration of diabetes were included in the regression analysis with log(e) (ln) of PON1 mass as the dependent variable. A regression model including PON2 Ala148Gly genotype, HDLC, and ln cystatin C explained 25.8% of the variance in PON1 mass. Conversely, waist, age, ln HbA1c, ln duration of diabetes, and ln PON1 mass, but not PON2 genotype, explained 38% of the variance in cystatin C. Subjects with cystatin C estimated glomerular filtration rate (eGFR) <60 ml/min per 1.73 m(2) (stage 3 kidney disease) had significantly lower PON1 mass compared with subjects with cystatin C-eGFR >60 ml/min per 1.73 m(2). The lower mass of PON1, an anti-inflammatory HDL-associated enzyme, in T2DM with cystatin C-eGFR <60 ml/min per 1.73 m(2) may contribute to their increased risk for cardiovascular disease.
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PMID:Association of the novel cardiovascular risk factors paraoxonase 1 and cystatin C in type 2 diabetes. 1915 17

The Schwartz formula was devised in the mid-1970s to estimate GFR in children. Recent data suggest that this formula currently overestimates GFR as measured by plasma disappearance of iohexol, likely a result of a change in methods used to measure creatinine. Here, we developed equations to estimate GFR using data from the baseline visits of 349 children (aged 1 to 16 yr) in the Chronic Kidney Disease in Children (CKiD) cohort. Median iohexol-GFR (iGFR) was 41.3 ml/min per 1.73 m(2) (interquartile range 32.0 to 51.7), and median serum creatinine was 1.3 mg/dl. We performed linear regression analyses assessing precision, goodness of fit, and accuracy to develop improvements in the GFR estimating formula, which was based on height, serum creatinine, cystatin C, blood urea nitrogen, and gender. The best equation was: GFR(ml/min per 1.73 m(2))=39.1[height (m)/Scr (mg/dl)](0.516) x [1.8/cystatin C (mg/L)](0.294)[30/BUN (mg/dl)](0.169)[1.099](male)[height (m)/1.4](0.188). This formula yielded 87.7% of estimated GFR within 30% of the iGFR, and 45.6% within 10%. In a test set of 168 CKiD patients at 1 yr of follow-up, this formula compared favorably with previously published estimating equations for children. Furthermore, with height measured in cm, a bedside calculation of 0.413*(height/serum creatinine), provides a good approximation to the estimated GFR formula. Additional studies of children with higher GFR are needed to validate these formulas for use in screening all children for CKD.
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PMID:New equations to estimate GFR in children with CKD. 1915 56

Glomerular filtration rate(GFR) can be estimated from serum (s-) creatinine using the modification of diet in renal disease (MDRD). However, its calculation is sometimes cumbersome in clinical use. Cystatin C is less influenced by age, gender and muscle mass than serum creatinine, and it has been proposed as an alternative marker for estimating GFR (eGFR). The comparison of s-cystatin C with MDRD-eGFR from 245 Japanese outpatients with chronic kidney disease (CKD)resulted in the equation of eGFR = 82.8/s-cystatin C - 10.7 (r = 0.85, n = 245). Based on this equation, there were 22 patients above + SD, which was the high-group in which s-cystatin C levels were higher than the corresponding eGFR, and there were 21 patients below -SD, which was the low-group in which s-cystatin C levels were lower than the corresponding eGER. Between the two groups there was no significant difference in age, gender, weight, and body mass index. The high-group included 1 case of hyperthyroidism and 7 cases of steroid user. The low-group included 4 cases of hypothyroidism and 1 case of steroid user. In healthy individuals, MDRD-eGFR is unsuitable for estimating GFR. Thyroid dysfunction or glucocorticoid excess are known to influence s-cystatin C levels. An improved eGFR equation was provided from 144 cases excluding 88 with normal renal function (eGFR > 90 mL/min/1.73 m2), 5 with thyroid dysfunction and 8 steroid users. eGFR = 86.1/s-cystatin C - 13.6 (r = 0.94, n = 144). Each GFR estimation provided from males or from females yielded nearly the same results as this equation. The prediction of eGFR using s-cystatin C may be convenient and useful in clinical practice, and the comparison of s-cystatin C with creatinine-based eGFR may reveal some factors that affect s-cystatin C or s-creatinine levels independent of GFR.
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PMID:[Comparison between serum cystatin C and estimation of GFR by the MDRD study equation for chronic kidney disease]. 1917 2

Although metabolic anomalies are often seen in advanced chronic kidney disease (CKD), their presence in more mild states is unknown. We studied 6722 participants in the Third National Health and Nutrition Examination Survey, dividing them into three mutually exclusive groups consisting of those having a normal or mildly reduced estimated glomerular filtration rate (eGFR) (Modification of Diet in Renal Disease (MDRD) formula), those with normal or elevated serum cystatin C, and those with clinically relevant moderate or severely reduced eGFR (stage 3 or 4 of CKD). The prevalence of several metabolic abnormalities associated with moderate to advanced CKD was determined after standardization for age, race-ethnicity, and gender. In the absence of stage 3 or 4 CKD, patients with elevated serum cystatin C had a higher prevalence of low hemoglobin and elevated uric acid, homocysteine, phosphorus, fibrinogen, and C-reactive protein than patients with a normal serum cystatin C. Our results show that in adults with normal or mildly reduced eGFR, elevated serum cystatin C is associated with an increased prevalence of metabolic abnormalities traditionally found in moderate or severe CKD. Elevated serum cystatin C may identify patients with 'preclinical' kidney disease not detected by traditional serum creatinine measurements.
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PMID:Metabolic abnormalities are present in adults with elevated serum cystatin C. 1929 2

Chronic Kidney Disease (CKD) is an important risk factor of the End Stage Renal Disease (ESRD). In this study, we investigated whether the protein to creatinine ratio (the ratio of P/C) determined by the semiquantitative urinary stick test and urinary sediments are useful for the early detection of CKD. One hundred sixty patients were classified to four or five groups by P/C ratio and various biochemical markers were analyzed. As a result, the 300 mg/g x Cr of P/C group showed a significantly increased serum cystatin C level. The positive rate of the P/C ratio in CKD stage was significantly increased compared with the conventional protein qualitative analysis. Further, the amounts of urinary sediments in CKD stage 1 to 2 were increased, such as hyaline cast, and pathological casts were increased in CKD stage 3 to 5. Thus, our present study suggests that the ratio of P/C and urinary sediments are useful for the screening of CKD.
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PMID:[Urinary protein to creatinine ratio and urinary sediments are useful for the screening of chronic kidney disease]. 1936 91

Antiphospholipid (aPL) antibodies are often detected in systemic autoimmune diseases. The aim of the study was to examine the correlation between the presence of aPL and certain markers of renal function in systemic sclerosis (SSc). Fifty patients (pts) with SSc were examined for the presence of antibodies to cardiolipin (aCL) and to anti-beta 2 glycoprotein I (a-B2GPI) in immunoglobulin M (IgM) and IgG class. Moreover, serum levels of creatinine, cystatin C, and glomerular filtration rate (GFR) were determined in all patients. In all studied pts together, three multiple-regression analyses were performed with one set cystatin C as a dependent variable, in the second GFR according to the Cockcroft-Gault formula and in the third creatinine clearance by Modification of Diet in Renal Disease (MDRD) formula. As independent variables, aPL of either type were inserted in addition to disease duration and age. IgG aCL was significantly positively associated with serum cystatin C (p = 0.002), significantly negatively associated with creatinine clearance according to the Cockcroft-Gault and MDRD formula (p = 0.01 and 0.02, respectively). IgG a-B2GPI was significantly negatively associated with creatinine clearance according to the Cockcroft-Gault (p = 0.03) and MDRD (p = 0.01) formula. IgM aCL and IgM a-B2GPI were not associated with any markers of the renal function. Our study suggests the relationship between kidney involvement and the positivity for some aPL in patients with SSc. Positivity for IgG aCL and IgG a-B2GPI in patients with SSc without secondary antiphospholipid syndrome seems to be connected with decrease of glomerular filtration.
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PMID:Antiphospholipid antibodies and kidney involvement in patients with systemic sclerosis. 1951 79


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